The neurons of the visual cortex are susceptible to rapid functional and structural organization in response to altered sensory inputs and injury. The precise mechanisms of this plasticity are unknown, however, several models have been used to describe this phenomena. One of these models is the Bienenstock, Cooper and Munro model, which incorporates a requirement for temporal overlap between activity in the pre- and postsynaptic cell. Fregnac et al.(1994) described a possible correlate for this model in vitro, termed covariance-induced potentiation (CIP), in layer II/III of the visual cortex. CIP can be elicited in visual cortical slices from both young and adult animals, however, the mechanisms of induction of CIP undergo a dramatic developmental change. Whereas CIP induction in the adult cortex requires activation of NMDA receptors, CIP in the young cortex can be induced independent of activation of the NMDA receptors. In both the adult and the young cortex, however, CIP induction is dependent on an increase in intracellular Ca2+. This suggests an alternative mechanism for the Ca2+ signal in young cortex. The objectives of this proposal are to determine the mechanisms responsible for CIP induction in the young cortex, and to determine 1) whether this parallel Ca2+ signal (in addition to the NMDARs) becomes uncoupled from the plasticity cascade during development, 2)whether the developmental switch in the mechanisms of CIP induction is due to a change in the total effective Ca2+ signal delivered to the neuron through activation of NMDARs or 3) whether the change occurs downstream from the Ca2+ signal in the plasticity cascade in the adult. I will employ a series of electrophysiological/ pharmacological analyses and Ca2+ imaging to determine the source of Ca2+ necessary for the induction of CIP in young cortex, as well as the nature of the developmental switch in the adult cortex.